View clinical trials related to Left Ventricular Hypertrophy.
Filter by:To evaluate the effects of paricalcitol capsules on cardiac structure and function over 48 weeks in patients with Stage 3/4 chronic kidney disease (CKD) who had left ventricular hypertrophy (LVH).
Chronic Heart Failure Analysis and Registry in the Tohoku District 2 (CHART-2 Study) is a large, prospective, hospital-based cohort study to investigate the following: - Characteristics of patients with chronic heart failure and prognostic risks of these patients. - Characteristics of patients with high risk for heart failure and critical factors which predict the development of symptomatic heart failure in these patients. - The incidence and prognostic impact of metabolic syndrome in patients with chronic heart failure. - The association between metabolic syndrome and the development of symptomatic heart failure.
The purpose of this study is to determine if the creation of a fistula or a graft plays a role in the development of heart disease for patients undergoing hemodialysis
The purpose of this study is to determine if using Eprex, to maintain hemoglobin within the normal range, will prevent or delay the progression of left ventricular mass growth.
The purpose of this study is to investigate effect of candesartan based therapy on percent change of B type natriuretic peptides(BNP) level in the subjects with hypertension and left ventricular hypertrophy.
The Dallas Heart Study (DHS-1) is a large, multi-ethnic, population-based epidemiological study designed to identify determinants of atherosclerotic heart disease (ASHD) in a representative United States (US) urban environment. This study completed enrollment in 2003. Our objective is to pinpoint factors contributing to progression: 1. from health to ASHD risk; 2. from ASHD risk to subclinical ASHD; and 3. from subclinical to clinical ASHD. Identification of the critical factors in these transitions will enable targeted implementation of appropriate therapy to interdict before clinical ASHD develops.
The consequence of aortic valve stenosis (AVS) is increased pressure load on the left ventricle which causes left ventricular (LV) hypertrophy, and myocardial stretch will cause activation of cardiac peptides and activation of the renin angiotensin aldosterone system (RAAS). The consequence of LV hypertrophy is increased chamber-stiffness and delayed active LV relaxation which initially will cause diastolic and later systolic dysfunction. In heart failure (HF) and ischemic heart disease the degree of diastolic dysfunction has been demonstrated to correlate with functional class, neurohormonal activation and prognosis which also recently have been suggested for AVS. With longstanding elevated filling pressures the left atrium (LA) will dilate. Only limited data are available on the degree and importance of LA dilatation in AVS. When apparent, symptoms of HF in AVS are associated with high mortality rates. If LV systolic dysfunction also is present prognosis will deteriorate further. In these cases aorta valve replacement (AVR) is recommended. AVR will normalize pressure overload and thereby decreases LV hypertrophy. Previously it was believed that in time LV hypertrophy regressed towards normal and even normalized. Recent studies however have demonstrated that LV hypertrophy regression mainly happens during the first year after AVR, and little subsequent changes are seen during the remaining 10 years. Furthermore, patients that experience most regression of hypertrophy have more favourable outcome and better functional class than patients with less regression of hypertrophy. Thus absence of reverse remodelling is associated with poor outcome after AVR. Importantly the regression of LV hypertrophy is closely paralleled by decreasing RAAS hyperactivity. RAAS hyperactivity may be attenuated pharmacologically with angiotensin II receptor blockers (ARB) which in systemic hypertension with LV hypertrophy has been associated with reverse remodelling. The hypothesis is that in patients undergoing AVR for symptomatic AVS, 12 months post operative blockade of the angiotensin II receptor will accelerate LV and LA reverse remodelling, reduce filling pressures and suppress neurohormonal activation compared with conventional therapy. This will lead to improved exercise tolerance and due to improved left atrial function reducing the risk of atrial arrythmias.
To compare the efficacy and safety of aliskiren in combination with losartan compared to losartan on the regression of the increased size of the left ventricle in overweight patients with high blood pressure.
Left ventricular hypertrophy (LVH) predicts mortality at start of dialysis. Prevention of of LVH is important. It is not known whether secondary hyperparathyroidism might induce LVH. In the present study patients are randomised to 1.25 dihydroxycholecalciferol or no treatment to study the effect on LVH.
Left ventricular hypertrophy (LVH) increases the risk of cardiovascular morbidity and mortality in patients with high blood pressure, compared to those without LVH. Reduction of left ventricular mass (LVM) with antihypertensive agents is associated with improved clinical outcome. This study will evaluate the effects of amlodipine/benazepril in reducing LVM in patients with high risk hypertension.